This middle-aged male with history of 3 previous stents, 2 in the RCA, had Syncope, Diaphoresis, Nausea, and Dizziness.
He called 911 and the medics recorded an ECG that looks just like his first ED ECG:
This ECG was texted to me (while out on a beautiful point on an island!) with the question: "Would you activate the cath lab?"
I responded: "Yes or at least get stat echo. It is 90% certain to be occlusion."
Outcome: The coronaries were clean. The troponins were negative. The subsequent ECGs did not evolve (this latter is the best evidence that there was no MI, as transient ACS can have all of the following negative: Cath, troponins, and Echo).
It turns out that the patient had a similar false positive activation 1/2 year ago because this is his baseline ECG.
He must carry a copy with him wherever he goes!!
Sometimes you just have to have a false positive. You must activate anyway. You cannot let an ECG like this go without action unless you know it is the baseline.
If there is any doubt, it would be reasonable to find an old EKG and/or to get an emergent echo.
Pretest probability: This also points out (again) that when patients do not have chest pain, especially if they do not at least have dyspnea, the probability that their ECG represents a STEMI decreases considerably.
He called 911 and the medics recorded an ECG that looks just like his first ED ECG:
 |
| There is inferior ST elevation and reciprocal ST depression in I and aVL, with reciprocal T-wave inversion in I and aVL. |
This ECG was texted to me (while out on a beautiful point on an island!) with the question: "Would you activate the cath lab?"
I responded: "Yes or at least get stat echo. It is 90% certain to be occlusion."
Outcome: The coronaries were clean. The troponins were negative. The subsequent ECGs did not evolve (this latter is the best evidence that there was no MI, as transient ACS can have all of the following negative: Cath, troponins, and Echo).
It turns out that the patient had a similar false positive activation 1/2 year ago because this is his baseline ECG.
He must carry a copy with him wherever he goes!!
Sometimes you just have to have a false positive. You must activate anyway. You cannot let an ECG like this go without action unless you know it is the baseline.
If there is any doubt, it would be reasonable to find an old EKG and/or to get an emergent echo.
Pretest probability: This also points out (again) that when patients do not have chest pain, especially if they do not at least have dyspnea, the probability that their ECG represents a STEMI decreases considerably.
Dr. Smith
ReplyDeleteAt my institution, a cardiology performed TTE takes at least 30 mins to an hour. Is this a reasonable time to wait if you have an equivocal case?
Daniel,
DeleteWhen it is not clearly a STEMI, you are not bound to the usual limits on door to balloon time, so that is really ok.
Steve
Hello Dr. Smith, great event as usual. I thank you for the opportunity you give me to improve my knowledge.
ReplyDeleteI agree with what you say consider this STEMI until proven guilty
How can we explain the ST-segment elevation in the inferior leads?
Early repolarization "aspect smile" ST segment? usually in cases of early repolarization in inferior leads we also have ST elevation in V5 V6.
But especially in the depression on aVL directs us to consider this an inferior STEMI.
We also see a ST depression in aVR and this is with the direction of the vector ST. Thank you .
Greetings from Italy. Vittorio
Vittorio,
DeleteAlways good to hear from you.
I do not have a good explanation for this ECG.
There are anomalies in everything, right?
Steve
Interesting
ReplyDeleteSo what may cause such changes ?
The STE is the same amplitude as R in inferior leads with reciprocal changes this points there is injury current isn't it ?
Thanks ..
I just don't have a good explanation!
DeleteWhat about tattoo ;-) ?
ReplyDelete???? Sorry I'm too dumb to understand the joke!
DeleteSteve
NICE case. This is a “false positive” that I do NOT feel bad about — since if all one has is this ECG in a patient of a certain age who has a history of coronary disease — one has to assume there is an acute RCA occlusion in progress. One of course “has to be there” for optimal decision-making … — and given this patient’s prior history of 3 prior stents (2 in the RCA distribution) — if the history was not truly suggestive of a new acute cardiac event — one might spend the no more than a few minutes needed to access a prior tracing for comparison … As per Dr. Smith — this should no longer be a problem in the future once this patient is given a wallet-sized copy of his “baseline” ECG to from this-time-forth carry with him on his person.
ReplyDeleteFrom a pure ECG point of view — IF the history was new-onset worrisome chest pain — I’d be suspicious of acute proximal RCA occlusion with RV involvement — because despite the artifact, it looks like there is slight-but-real coving of the ST segment with positive T wave in lead V1. Given how hyperacute the inferior ST-T waves appear to be, I would expect anterior ST depression UNLESS this was being attenuated by ST elevation due to associated RV infarction.
That said, I’d want to verify lead placement — given a bit more negative P component in V1,V2 with somewhat unusual QRS morphology in lead V1 (that typically shows a more negative S wave). Of course, given what we subsequently found out about this patient — we can explain the limb leads as this patient’s “baseline” — with the R > S in V1 with positive T waves in anterior leads due to residual change from prior posterior involvement … Just goes to show how important the History and prior tracings may be in certain cases — as well as how important it is to “put all pieces of the puzzle together” in clinical decision-making. THANKS for presenting this insightful case!
Thanks, Ken!!
DeleteGreat case for my students!
ReplyDeleteThanks,
Jon Woodson
Interesting, I would probably have done the same, and then come back to the ECG. At J point, in II, compared to TP, J point is close to TP line, but about 1 mm when compared to PR. In III, you have a true 1 mm. In AVF, I would call for a 0.5 mm elevation compared to TP, a bit more when you compare to PR. And of course, some (mild) mirroring in AVL. So, when you look carefully, you don't have AHA 2013 criteria for diagnosis of MI... although it looks quite as MI starting. So I guess the right call would be STAT echo if you can, closely repeated ECG and trops.... and see, instead of activating. That's even more important with the"hard" decision, which would be to go for lysis if you're not close to a PTCA center.
ReplyDeleteThis bring on the interesting question about what's the baseline for evaluation of J / ST elevation? I teach always the TP as the good landmark for ST elevation, exactly because such ECGs.
Alain,
DeleteST elevation criteria are really simply inferior to subjective interpretation.
Check out Massel D. Am Heart J 2000;140:221-216.
Thus, the means of measurement are not that important.
I have showed also how no lytic trial ever specified method of measurement in STEMI. We don't even know what is the best enrollment criteria for such trials: onlinelibrary.wiley.com/doi/10.1197/j.aem.2005.10.019/pdf
Steve
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ReplyDelete